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Gregory Marcus
President, Chief Executive Officer & Chairman, MARCUS CORP

Update AF: DECAF (Coffein & AF) / CABG-AF - Dr. Gregory Marcus and Dr. Florian Herrmann

🎥 Nov 24, 2025 📺 MARKUS at HOMe ⏱ 43m 👁 148 views
Dr. Gregory Marcus (San Francisco, CA, USA) and Dr. Florian Herrmann (Munich, Germany) present two landmark studies on atrial fibrillation, namely DECAF on coffee consumption in patients with atrial fibrillation and CABG-AF on new-onset atrial fibrillation after coronary artery bypass grafting. Dr. Greg Marcus is Professor of Medicine at the University of California, San Francisco (UCSF), Associate Chief of Cardiology for Research at UCSF Health, Endowed Professor of Atrial Fibrillation Research and Associated Editor of JAMA. Dr. Marcus is Principle Investigator of DECAF. Dr. Florian Herrman...
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About Gregory Marcus

Gregory Marcus, President, CEO, and Chairman of The Marcus Corporation, appeared on two podcasts in July 2026 to discuss the company's focus on in-person experiences, leadership, and the changing film industry. On the "Making New Possible" podcast, Marcus stated that "humans are meant to be together" and that "we are stronger in being together," framing this belief as central to his company's movie theater and hospitality businesses. He also said, "If you have the capability, you have the responsibility," adding that those who have been given much should help take care of others. On the "Techad" podcast, Marcus noted that Warner Bros. has reduced its annual film output from 24 to about 12 films, attributing the decline to the studio's need to allocate capital across multiple business lines including HBO. Marcus discussed his personal involvement in the company's social media presence, saying he follows the advice of "some 20-year-olds" on platforms like TikTok. He described his on-screen appearances in theater pre-shows, including promotional pieces with actors Kevin Costner and the cast of "Super Troopers." Marcus also reflected on his leadership philosophy, stating that he aims to surround himself with great people and that he believes in being patient because "things are cyclical."

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Transcript (26 segments)
H
Host0:07
Dear colleagues, in partnership with Theologus at home, we welcome Dr. Gregory Marcus in San Francisco, California, USA, and Dr. Lian in Munich, Germany, for an update on atrial fibrillation with two very important studies published by our two guests very recently: DECAF on coffee consumption in patients with atrial fibrillation, and the Munich study on new-onset atrial fibrillation after coronary artery bypass grafting. Dear Dr. Hammer, we are very happy to host for the first time a heart surgeon at home, and dear Greg, welcome back at Marcus at home after our 2022 webinar on alcohol and coffee intake in atrial fibrillation. Happy to have you back.
G
Gregory Marcus0:55
Thanks for having us.
H
Host1:01
Thanks for joining also from my side. As a brief introduction, I think Dr. Marcus doesn't need much of that. He's an endowed professor in atrial fibrillation research, probably the leading working group when it comes to the effects of caffeine and alcohol on atrial fibrillation, and recently published studies on that. That's where we come together here. Also, a study that was presented at the American Heart Association meeting. Professor Marcus is Associate Chief of Cardiology for Research at the University of California, San Francisco Health Institute, and he's Associate Editor at JAMA as well. As I said, his research interest is atrial fibrillation, and he's conducted numerous trials on that. We are very happy to have you here again and hear some of your thoughts on the most recent one, the DECAF study, and also maybe hear your comments which you published as an editorial on the study by Florian Hammond and Dr. Dr. Herman. Thank you for coming. We are very happy to have a heart surgeon in this round for the first time. Dr. Hammerman has quite some research achievement and won prizes and got research funding from the KUNAR Forinius, and recently last year was awarded a PRIME Advanced Clinician Scientist Booster Award to facilitate his research next to his clinical duties. We are very keen to hear your presentation on the CABG-AF study on atrial fibrillation post-bypass surgery. So without further ado, I would ask you, Dr. Marcus, first to start with your presentation. The floor is yours.
G
Gregory Marcus2:48
Thank you. Again, a pleasure to be here and talk about our study, and I look forward to talking with Dr. Herman about his study. This one is our Does Eliminating Coffee Avoid Fibrillation or DECAF trial that we were privileged to present at the AHA and recently published. Of course, conventional wisdom is that coffee caffeine leads to more tachyarrhythmias. This is what we were at least frequently taught in medical school, and many patients are warned against consuming caffeine, especially those with fast heart rhythm. Our journey here began several years ago where we conducted this observational study using data from the UK Biobank. We just looked at how much caffeinated coffee hundreds of thousands of people in the UK consumed at a baseline state and followed them over time to see what their risk was of various tachyarrhythmias. This is a figure showing all of those tachyarrhythmias combined, and we were quite surprised to find this very consistent inverse relationship. So the more caffeinated coffee an individual described consuming at baseline, the lower the risk of incident tachyarrhythmias. When we teased out what fast rhythms were really contributing here, it was primarily atrial fibrillation. We recognize that as an observational study, this is of course prone to confounding. So maybe there's something different about the type of people who decide to consume caffeinated coffee that's the true causal operator. We then thought about how we can apply randomized control trial study designs that we know are the best way to mitigate against confounding. This led to our CRAVE trial: Coffee and Real-time Assessment of Atrial and Ventricular Ectopy. I enjoyed describing or discussing with you all on this forum a few years ago where this was just a day on versus off randomized caffeinated coffee consumption. Our primary outcome was the frequency of premature atrial contractions, which we know are a really potent predictor of atrial fibrillation, and we found no relationship between caffeinated coffee consumption and PACs. Now importantly, as a kind of broad-strokes big picture context limitation or consideration related to our DECAF trial, I will get back to in a moment. We did find more premature ventricular contractions on days when people were randomly assigned to caffeinated coffee. So that is certainly worthy of consideration, especially for people who suffer from PVCs, and certainly also worthy of further investigation as that was a secondary endpoint. So then of course we wanted to know, okay, how about atrial fibrillation itself? We conducted this DECAF trial. Chris Wong, who was a fellow with us in cardiac electrophysiology, now actually already full professor at the University of Adelaide, began work with me on this when he was a fellow with us. He subsequently went to Adelaide. We were able to enroll 200 patients with persistent atrial fibrillation from UCSF, University of Adelaide, and Chris Chung, also a former UCSF fellow now in Canada. We only enrolled people undergoing electrical cardioversion or scheduled for electrical cardioversion of atrial fibrillation, and we did this for a couple reasons. One, it assured that their atrial fibrillation was clinically relevant. It was important enough that some treating physician decided you need a procedure for your AFib. We need to get you out of atrial fibrillation. Two, it gave us a common starting point where everyone was starting in sinus rhythm. They didn't need to actually undergo the electrical cardioversion because we know sometimes people are started on antiarrhythmic drugs and they show up in sinus rhythm, and we didn't want to exclude them. Another important inclusion criterion was people had to have consumed caffeinated coffee at some regular time in the last 5 years. So they didn't need to be consuming caffeinated coffee when they were enrolled because we know a lot of patients stop consuming caffeinated coffee, not because it caused a problem, but because their treating physician instructed them to do so, and we wanted to make sure to include them. They couldn't have had recent CT surgery, which is obviously relevant to Dr. Herman's study he will tell us about, nor could they have had a recent ablation or plan to change their management in the next 6 months. They were randomly assigned to try to consume a cup of caffeinated coffee a day at least, you could consume more if you want, versus try to avoid all coffee and all caffeine for six months. Our primary outcome was a recurrence of clinically relevant atrial fibrillation, meaning they needed to have a diagnosis of atrial fibrillation recognized by a treating provider and documented with some ECG evidence of atrial fibrillation including from a wearable monitor. These are the results. On the left is what happened to actual coffee consumption. Both groups started, and you can see these kind of dark lines in these box plots are the medians. Interquartile range are the boxes, and then the larger range in the y error bars. But if you focus in on the medians, it's about a cup a day. In the group randomly assigned to coffee consumption, median amounts remained about a cup a day. There were some outliers in those randomized to abstinence. Sometimes people did consume some coffee, but the median was actually zero cups of coffee in follow-up. This was ascertained at 1 month, 3 months, and 6 months and remained fairly consistent. In our main analysis, primary outcome, we found that those randomly assigned to caffeinated coffee abstinence actually experienced a significantly higher risk of AFib recurrence. So those randomly assigned to caffeinated coffee consumption appear to experience a lower risk of incident atrial fibrillation over those six months. Those are all my slides, and I look forward to discussing more with all of you.
H
Host9:31
Well, maybe give the word to Dr. Herman first if you like. We have some particular questions maybe.
D
Dr. Herman9:38
Thanks. I read the publication online and I was impressed. It was a very interesting trial, and that's definitely shown by the amount of views it's already received, almost 150,000 views, which is spectacular. It's very interesting. It's also related to cardiac surgery a little bit because it's the same recommendation that we frequently make as well about caffeine, and I think a study in this area might be interesting as well in the future because there's no actual data that's related to caffeine intake after cardiac surgery. I haven't found any yet. We still make the recommendation that patients shouldn't be drinking caffeinated coffee after surgery. So that's one interesting thought. I saw that looking deeper into your data, I saw that the proportion of patients in each group that had a certain amount of specific medications were very similar. Is that something that you stratified in randomization?
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Gregory Marcus11:03
We did not. We stratified by site. Use of medications may have traveled a little bit by site. We were fortunate that randomization thankfully kind of balanced that out. It's almost perfectly balanced in the groups.
D
Dr. Herman11:14
And my second question is about the topic clinically relevant AF because I did a lot of research in this study on subclinical AF, which I didn't expect before, but it developed. The more data came in, you saw it was much more subclinical AF than clinical AF. How would that be something that you're interested in, also with caffeinated drinks?
G
Gregory Marcus11:50
Yes. It's a limitation of the study, but also I think just important in understanding the implications. It was designed to be quite pragmatic. We would have loved to have put loop recorders in everyone as in your study, but we didn't have the resources in this particular study. I will say this study was also quite difficult to convince patients to participate in. If you look at the consort diagram, there's a pretty big drop off between the thousands of people we talked to compared to those that ultimately were randomized. The most common reason being many people didn't want to give up their coffee. In fact, we initially when we started, we had hoped to do this for a year and then realized people are really just not going to do it for a year. So let's truncate it to 6 months, which thankfully was sufficiently powered. Some number just didn't ever drink caffeinated coffee. But yes, the clinical relevance did mean they had to present with atrial fibrillation, have a diagnosis of atrial fibrillation, and so almost certainly there's subclinical atrial fibrillation going on. It would be very interesting to determine that. To put on a really skeptical lens, it would be not unreasonable to say, well, maybe the people who were consuming caffeinated coffee just felt a little better and they were less likely to complain to their doctors.
D
Dr. Herman13:20
That's the exact thought I had.
G
Gregory Marcus13:27
Yeah. So that could be the case. And then it becomes an issue of what is the research question and what is a mediator versus a confounder. So if your outcome is healthcare utilization for AFib, it still is reducing that. It's just the mechanism by which it's doing it is not necessarily suppressing the AFib itself. We actually think, you know, a common question I get is, does this even make sense mechanistically from a biological standpoint? Does it make sense that caffeine or coffee might suppress AFib? There are actually several potential biologically plausible mechanisms. One is that most atrial fibrillation is probably vaguely mediated, and interestingly, presumably the post-cardiac surgery may not fall into that category, but the more spontaneous forms are. So maybe the sympathetic effects of caffeine actually help suppress AFib. Caffeine blocks adenosine. We know from our experience in the EP lab, adenosine triggers AFib. So maybe it's protecting it that way. Animal models have shown that caffeine tends to prolong left atrial refractoriness. That is an electrophysiologic property that has been shown to prevent AFib. That's how sotalol works. Dofetilide, amiodarone are probably suppressing AFib by prolonging left atrial refractoriness. Then, kind of a little bit longer term, there's very good epidemiologic evidence, although not randomized control trial evidence, that people that consume caffeinated coffee experience a lower risk of diabetes, and for reasons we don't completely understand, diabetes predicts AFib even after adjusting for sedentary behavior and BMI. Finally, there's good data such as from Prash Sanders' group that physical activity can reduce AFib. And we showed in our CRAVE trial that when people were wearing Fitbits, when they're randomly assigned to caffeinated coffee, they exercise more. So maybe that's a pathway that might lead to a lower risk of AFib. So it's not as if we are free of potential mechanisms, and the finding does fit with observational evidence. But to be scientific, we have to always put on our skepticism hats, and that's how we arrive at the truth. We chip away at things and consider all the possibilities.
H
Host15:59
Before we give the word to Dr. Herman for his presentation, one question I have: obviously we have to rely on the statements of the patients concerning their coffee use. I was so impressed in your alcohol study that you provided people with a wrist alcohol measurement tool, which is obviously not available for coffee. Is there any humoral factor that we could measure, any toxicological screening that was not only in your study? I understand.
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Gregory Marcus16:30
Yeah, I think if we had serum samples, theoretically we could have. There is not, you're right. We have an ongoing study using alcohol. The probably most reliable now is an ankle-worn sensor, which then brings up issues of stigma and things like that. But yes, we've been very interested to try to prove the exposure. Our suspicion is that if self-report was inaccurate, presumably it would be on the side of drinking more than they acknowledged, which then presumably would have more reduced our power rather than created a spurious false positive. In CRAVE, we did a few things. We used our geolocation tracking where we showed that people visited coffee shops more often when they were randomized to coffee. We had them press a button on the Ziopatch when they consume coffee to try to mitigate against recall bias. And in CRAVE, we told all our participants, 'We'll pay for all of your caffeinated coffee as long as you give us a receipt with a date on it, whether you were supposed to or not.' And we did find that actually people seemed to be quite compliant. There is this thing called the Hawthorne effect, this effect where if someone knows they're being watched, they're more likely to adhere. Maybe we didn't have that in DECAF, but that is another important potential limitation. Certainly, these are all great ideas for future research.
H
Host18:02
I would have two final questions, Stefan, if I may. The first surely is this is an international study. So do you have any information whether the caffeine content of the different coffee preparations that people receive in the States versus Australia does differ? Surely because the number of coffees per day is quite low in your study, I guess because people who drink a lot of coffee like me are not really willing to participate in this kind of study. And the second question would be there's quite a lot of people who actually had cardiac devices, so in whom you would have 24-hour or so rhythm controls. So if you compare these two groups of people, truly not randomized, those who just have clinical AF versus those with cardiac devices, do you see any difference here?
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Gregory Marcus18:57
Yeah, so I'll try to answer that first one first and then circle back to the very good question which actually has some interesting implications. When we looked at people who either had an implantable device, which was a small number, or were for whatever reason prescribed a wearable ECG monitor, all the findings are very consistent. In fact, they're even stronger. And it turns out that more people in the caffeinated coffee arm at some point wore an ECG monitor without any AFib, which we thought was somewhat reassuring in terms of differences across international sites. You're right. So I have a few things to say there. Number one, I was recently at a symposium at UC Davis, which is, as you may know, a big agricultural university, very interested in the science of the biochemistry of plants and things like caffeine. They shared evidence from a recent study where going to the same Starbucks, ordering the same drink, same size, they actually measured how much caffeine across different days there was in that drink, and there was a huge variation. So that's same country, same shop, same drink. So yes, there's a lot of variability. Now also importantly, on a larger magnitude scale, we all metabolize caffeine at different speeds. That's genetically determined, it's also determined to some degree how much we tend to drink, and it's very likely that people sort of self-titrate. We actually found this in the UK Biobank where we looked at genetic variants that determine caffeine metabolism related speed, and people who consume caffeine more quickly drink more caffeinated coffee. So it may be that the amount of caffeine that's actually being exposed to the heart is somewhat equalized. And then finally, I will say that another important consideration in this study is of course we cannot disentangle effects that might have been due to caffeine versus things in coffee. Coffee itself, and I didn't have a chance to mention this, is anti-inflammatory. We know that this almost certainly is related to open heart surgery related AFib, probably a lot of that is kicked off by inflammation. The same has been shown in the general population that people with a higher C-reactive protein have a higher risk for AFib. So maybe this is less related to caffeine and more related to coffee. So a study of decaf coffee truly might also be worthwhile pursuing in the future.
H
Host21:35
Is that the reason why you also included decaf in the substance that's not allowed in that group?
G
Gregory Marcus21:46
Right. That's right. We wanted to at least hone in on caffeinated coffee, which remains, you know, a lot of people drink decaffeinated coffee, but most people who drink coffee drink caffeinated coffee. So we wanted to capture that real life experience, recognizing we could not separate out effects that mechanistically were related to caffeine versus coffee itself for now.
H
Host22:11
All right. Well, thank you. And speaking of real life medicine, Dr. Herman, if we may ask you also to share your slides and show us some of the real life randomized data that we are very keen on and a terribly interesting study for looking after our surgical patients.
D
Dr. Herman22:29
First of all, thanks for inviting me to present our study from Munich. I'm honored to be a guest here, especially together with Dr. Marcus, who's a great researcher in the field of arrhythmias, and also I've seen the kind of people that were invited to your talks, and it's really great. So we performed the CABG-AF study in Munich, investigating long-term continuous monitoring of new onset atrial fibrillation after coronary artery bypass grafting. It's a prospective multicenter study. We're funded by the Clinical and the German Research Foundation. The background is the incidence of new onset atrial fibrillation after CABG is around 30% based on registry studies. There's quite a bit of variability, but in large registry studies it says around 30%. The incidence is mainly based on data from telemetric monitoring and intermittent rhythm monitoring and mainly until hospital discharge. So in most studies, time frames didn't extend far past discharge, sometimes up to 30 days, but not much more than that. The current ESC/EACTS guidelines recommend long-term oral anticoagulation should be considered in patients with new onset AF after cardiac surgery. It's a class 2A recommendation. It's a similar recommendation in America in the ACC guidelines. There are a couple issues in our view with these recommendations. First of all, the words 'long-term oral anticoagulation' and then also the fact that it's cardiac surgery and it's not specific types of cardiac surgery because we know that there are differences between different types of procedures and different cohorts of patients. That's the background. The aim of our study was to determine the incidence and the burden of new onset AF in the first 12 months after CABG. It was an investigator-initiated prospective observational study of AF using continuous monitoring in two cardiac surgery centers. We actually planned more centers, but it's such a difficult methodology that it couldn't be expanded much more than two centers. The inclusion criteria were first time isolated CABG for three vessel disease or left main disease, no history of AF or other arrhythmias, and a preoperative left ventricular ejection fraction over 35%. We excluded concomitant cardiac surgery. We just wanted to look at CABG, and we excluded mechanical circulatory support at weaning from bypass. AF was defined based on the algorithm of the implanted monitor at two minutes of AF. The timeline of the study was practically that monitors were implanted at the end of surgery, monitoring started at the end of surgery, continued for one year for the primary endpoint, and then continues until 3 years after surgery. After the three years or after battery depletion, the insertable cardiac monitor can then be removed. Our cohort ended up being 198 patients, with one patient where data collection couldn't be started because the patient died before the whole monitor was initialized. So at the end, we had 197 patients with monitoring data. 25 patients were female, around 13%. It's similar in most CABG cohorts. It's primarily men, which is a limitation of the study. The mean age was 66, which is a typical age for bypass surgery in most cohorts as well. Diabetes was around 40% of patients. A lot of three vessel disease, 50% around left main disease, and primarily bypass surgery on pump, only around 24% off pump surgery. The results: the primary endpoint was the cumulative incidence of new onset AF, and that's shown on the graph on the left. You see that around 48% of patients developed AF in the first year after surgery. That's 95 of the 198 patients. We had a median episode length of 6 minutes, median time to AF or to first AF episode of 3.3 days, and 63% of the episodes were asymptomatic. 67 were not detected in standard monitoring, and the cumulative incidence of AF detected with standard monitoring was around 34%. Here you see the AF burden within the first 12 months after CABG. You see that it's primarily AF in the first weeks, two weeks after surgery. The median AF burden during the first 12 months was 0.07%, which corresponds to 6 hours and 10 minutes of AF. In 90 of the 95 patients who developed AF, the incident episode occurred within the first month, and 77% of the time an AF occurred within the first 30 days after surgery, which you can see in the inset up here showing that most of the AF is in the first month. Here you see an increased burden that's unexpected after 9 months. That's one patient with persistent AF for a time after surgery. If we look at the AF burden by time frame, we see that in the first seven days after surgery, we have a median AF burden of 3.65%. Days 8 to 30, it's 0.04%. And numerically calculating the AF burden, the median burden is 0% after 31 days. There are patients with AF, but if including all the patients, you calculate a median AF burden of 0%. Of the 90 patients with incident episodes in the first 30 days, 19 experienced recurrence after 30 days. That's 21% of the patients, and the median episode length of recurrent episodes was 4 minutes. 97% of recurrent episodes were not detected in standard monitoring. If we look at the episode lengths, we see that most episodes are quite short, under an hour, and only 15 episodes had a length greater than 24 hours. We know this length greater than 24 hours for subclinical AF is relevant because in the ASSERT trial, they found that the stroke risk is higher for subclinical AF with a length greater than 24 hours, and that's why we looked at that specifically. Of the patients who developed these episodes lasting greater than 24 hours, eight had these episodes prior to discharge, and three patients had these episodes after discharge. Before discharge, the episodes were detected in standard monitoring, and after discharge, they weren't detected in standard monitoring. So in conclusion, the incidence of new onset AF in the first year after CABG is higher than previously reported. The AF burden is very low, especially later than 30 days, and given the known bleeding risk with oral anticoagulants, the very low burden questions the current guidelines recommending long-term oral anticoagulation. In our opinion, if oral anticoagulation is initiated for new onset AF, the indication should be reassessed within the first 30 days. Most patients shouldn't be receiving anticoagulants, and if they do, there should be a reassessment. A lot of the data shows that even a year after surgery, patients still have anticoagulants that were started early after surgery. It kind of suggests that once it's started, it's not stopped, and that could be a long-term issue in these patients. That's why we want to motivate people to reassess the actual indication for the medication. So that's the CABG-AF study for you.
H
Host32:07
Well, thank you so much. As mentioned, terribly interesting, very clinically relevant, especially in an outpatient setting where we see patients now after CABG weeks and months and years afterwards, and as you said, often still on anticoagulation. Dr. Marcus, you wrote a terribly interesting editorial on that, and I'm sure you'd be happy to ask some questions, comments.
G
Gregory Marcus32:34
Yeah, thank you, and congratulations Dr. Herman on a great study. I think there are many implications. In my mind, there are two main ones. One is kind of a conceptual, very broad implication related to atrial fibrillation on the whole. The second is more practical and specific to the post-operative setting. In the more broad context, there is a trend that I think is very appropriate to recognize that when people have AFib due to what previously may have been considered reversible causes, we should assume that actually those people probably are going to have it again, such that we should anticoagulate them. For example, someone comes in the hospital with pneumonia and they're found to have AFib, or even maybe even sepsis, they're found to have atrial fibrillation while on the monitor, and the tendency is often to assume, well, they're really stressed, this is an unusual circumstance, maybe we shouldn't really burden them with long-term anticoagulation. But the data suggests that no, in fact, those people are just showing you that they are prone to atrial fibrillation. They're going to be stressed again, and maybe the reason you caught it was because they're now on a monitor and you just didn't see it before, and almost certainly it's to the benefit of those patients to assume they're going to continue to have atrial fibrillation and initiate oral anticoagulation. So if that's the direction things are going, a reasonable question is, can atrial fibrillation ever be truly reversible? And the best candidate would seem to be the post-operative setting, and Dr. Herman's important contribution here is to demonstrate that yes, it really can be reversible. The other thing that often comes up, and this is relevant to this study as well, is what duration of atrial fibrillation matters in terms of stroke thrombotic risk. The issue is when someone has spontaneous atrial fibrillation and we find, oh, here they just had 5 minutes of atrial fibrillation, but it happened spontaneously, I think it's safe to assume that that atrium is going to continue to remodel and probably over time that person's going to experience more and more atrial fibrillation. But in the setting of open heart surgery, you have an insult that is itself very likely responsible. And again, this current study demonstrates yes, if you put loop recorders in, the great majority of atrial fibrillation goes away. So I think the conclusion is, yes, atrial fibrillation can be reversible. This is one situation where that is proven, and we shouldn't apply this other assumption that they're always going to be at risk for atrial fibrillation in this particular setting. Then the other implication has to do with anticoagulation and the duration of anticoagulation. What should we do? I'm curious to hear how Dr. Herman thinks we should really apply this in practice. I know you mentioned maybe after 30 days. I wonder if there's a because DOACs in particular, apixaban for example, tends to be pretty safe. I certainly would still recommend obtaining a monitor afterwards, and I would say sometime within that year. I think the clear evidence here is these patients should not be considered for long-term anticoagulation, meaning for the rest of their life. So we should think about monitoring them with the goal of stopping the anticoagulation. So I'm curious, Dr. Herman, I think maybe two questions. One is what is your current recommendation for the duration? And number two is your feeling, given these data, that actually these patients should have loop recorders implanted to guide it, or do you think we can rely on external monitors?
D
Dr. Herman36:41
Those are both quite difficult questions. That's one limitation of our study. Obviously, we didn't test does the loop recorder improve anything for the patient, right? And we didn't test what the length of anticoagulation should be. Those are two questions we can't really answer with the study. But we did collect some pathophysiological background that can be maybe extrapolated, but it will never really be able to answer these questions. That has to be answered with a randomized trial. There is currently a randomized trial that's investigating this issue. It's the PACES trial that's looking at three months of anticoagulation combined with antiplatelet therapy for post-operative AF after CABG, which is currently including patients. So I think we have to wait for that trial to really be able to answer that question. Most data suggests that around 25% of patients that have POAF that's been detected actually receive anticoagulants, and it's pretty stable and similar in different regions of the world from what I've seen from the data. It was similar in our trial. It was around 27% of patients that received anticoagulants. Interestingly, we did not have an effect on or we didn't decide whether patients were anticoagulated or not. That was decided by the treating physicians. But we obviously provided the information of whether they had AF or not. And at the end of the first year, a similar amount of patients still were anticoagulated. So that kind of shows what the current situation is. What I would recommend is patients with a high burden of AF should probably be considered for anticoagulation. And in these patients after 30 days, you should see if they still have a high burden of AF. From the data that we have, most almost all will not have the high burden, and you should probably discontinue the anticoagulation. But obviously, there's no hard data available to answer this question.
H
Host39:34
I have one question actually before we have to look at the time. Obviously, it's a study on CABG as you said. Can you, I know we can't extrapolate, but what's your thought on real open heart surgery? So not only opening thorax and putting them on a machine, but also incising the left atrium for mitral valve surgery. Would you believe that's a different story? I mean, many mitral valve patients have AF anyway, but if they hadn't had it before the operation and they start afterwards, we'd probably keep them on anticoagulation, wouldn't we?
D
Dr. Herman40:05
That's a very good question. If you look at the inclusion and exclusion criteria of our study, we tried to involve this idea that patients are very different even in a specific cohort. So we excluded patients with reduced ejection fraction especially for this reason, and also patients with preoperative AF especially for this reason, because we wanted a clean cohort where we can actually make a comment about how much AF these patients had. And if we look at different types of cardiac surgery, it gets even more important. CABG patients have a lower risk of AF postoperatively compared to patients with valvular surgery. That's what registry data tells us. I think that's an important fact also for the guidelines. So my recommendation would be that this should also be considered in the guidelines when recommending how to treat these patients after surgery. There are some studies that have shown that the stroke risk in POAF after valvular surgery might be higher than that after CABG.
H
Host41:33
Thanks so much to the two of you. I believe 2025 has been another amazing year for atrial fibrillation research with important studies, surely including DECAF and CABG-AF. The findings are definitely important not only for cardiologists but also for other doctors in internal medicine like neurologists, since all of us see and care for these patients. We're positive that we will see more great data in 2026 from Munich, from San Francisco, and from elsewhere. We would love to see you back then with your new results. Until then, we will finalize our academic year next week with our top 10 of cardiology and lipidology 2025 in German language. Without disclosing the results too early, we will hear on coffee and atrial fibrillation again. So stay tuned, and we wish Merry Christmas and a happy 2026 in Bavaria, in California, and everywhere else. Thank you.
G
Gregory Marcus42:27
Thank you so much.